Can tricuspid regurgitation cause fatigue?

Does Tricuspid Regurgitation Cause Fatigue?

Yes, tricuspid regurgitation definitively causes fatigue, which is one of the cardinal symptoms of this condition and results from low cardiac output and impaired oxygen delivery to tissues. 1, 2

Mechanism of Fatigue in Tricuspid Regurgitation

Fatigue in TR develops through a well-defined hemodynamic pathway:

• Reduced cardiac output is the primary mechanism, as TR causes inefficient forward blood flow and decreased systemic perfusion 1, 2
• Impaired exercise capacity occurs because patients with severe TR demonstrate significantly lower peak oxygen consumption (VO2) and reduced pulmonary blood flow during exertion 3
• Inadequate left ventricular filling paradoxically occurs despite elevated right-sided pressures, as ventricular interdependence causes the dilated right ventricle to compress the left ventricle and reduce LV transmural filling pressure 3
• Low cardiac output reserve relative to metabolic demands means patients cannot augment cardiac output appropriately with activity 3

Clinical Presentation Pattern

Fatigue manifests in a characteristic progression:

• Early symptom: Fatigue is often the earliest and most prominent complaint, appearing before other signs of right heart failure 2
• Exertional intolerance: Patients initially experience fatigue with physical activity, progressing to symptoms at rest as disease advances 1
• Associated symptoms: Fatigue typically occurs alongside weakness, general exertion intolerance, and reduced exercise capacity 1

Severity Correlation

The presence and severity of fatigue correlates with TR stage:

• Stage D (Symptomatic Severe TR): Fatigue is a defining feature, along with palpitations, dyspnea, abdominal bloating, anorexia, and edema 1, 2
• Progressive disease: More profound fatigue develops as right ventricular dysfunction and tricuspid valve regurgitation evolve 1
• Functional limitation: Fatigue contributes to marked limitation of physical activity (WHO Class III-IV) 1

Hemodynamic Evidence

Invasive hemodynamic studies confirm the physiologic basis:

• Patients with severe TR show lower pulmonary blood flow at rest (3.6 vs 5.1 L/min in controls) and during exercise (6.4 vs 10.3 L/min) 3
• Reduced peak VO2 (10.3 vs 13.8 mL/min/kg in controls) directly correlates with fatigue severity 3
• Impaired cardiac output augmentation with exercise explains exertional fatigue specifically 3

Clinical Pitfalls

Important considerations when evaluating fatigue in TR:

• Fatigue may be the only symptom: The classic systolic murmur may be inaudible even with severe TR, making fatigue a critical diagnostic clue 1, 2
• Multifactorial in advanced disease: Fatigue worsens as hepatic dysfunction develops from chronic venous congestion 1
• Atrial fibrillation contribution: Concomitant AF (present in 70-88% of severe TR patients) compounds fatigue through irregular rhythm and reduced cardiac efficiency 2

Prognostic Significance

Fatigue as a symptom carries important implications:

• Stage classification: The presence of fatigue places patients in Stage D, indicating symptomatic severe TR requiring intervention 1, 2
• Poor prognosis marker: Symptomatic TR with fatigue is associated with increased morbidity and mortality 4, 5
• Treatment indication: Fatigue from severe TR represents a Class I indication for surgical intervention when TR is addressed at the time of left-sided valve surgery 4